Insulinoma-associated 1 (INSM1) is a transcriptional repressor protein that is required for the development of the endocrine pancreas, adrenal gland, basal neuronal progenitor cells in the neocortex, and the monoaminergic neurons in the hindbrain (1). INSM1 expression is restricted to early fetal development in neuronal and endocrine tissues (2-6). One striking feature of the INSM1 mRNA is despite its absence in normal adult tissues, it is strongly expressed in tumors of neuroendocrine origin such as small cell lung carcinoma (SCLC), medullablastoma, neuroblastoma, medullary thyroid carcinoma, insulinoma, retinoblastoma, pheochromocytoma, and pituitary tumors (7-9). Using a transgenic animal model and in vitro reporter gene assays, the spatial and temporal expression of INSM1 has been demonstrated to be regulated by the 5′ 1.7 kilobase pair promoter region (10;11). The 1.7 kbp promoter region has been linked to a suicide gene for delivery into tumor cells. The ability of the INSM1 promoter to drive expression of the herpes simplex virus thymidine kinase gene selectively has been tested in small cell lung cancer (SCLC) cells and in pediatric brain tumors (12;13; see also, U.S. Patent Application Publication No. 2005/0037445). Adenoviral vectors are one of the most widely exploited viral delivery systems for gene therapy due to their ability to infect a wide range of host cells and the minimal risk associated with the use of a non-replicating form of the virus. The adenovirus genome is easily manipulated and with the deletion of the E1 and E3 genes allows for the incorporation of up to 7.5 kilobase pairs of exogenous sequence. However, one major drawback of adenovirus is host mediated immunity to the virus. In addition, due to the high liver transduction efficiency following intravenous delivery of adenovirus, the liver is most susceptible to toxic side effects.